Abstract

Chronic periodontitis (CP) is a complex pathology with a significant impact worldwide causing bone loss. Oral dysbiosis is a highly inflammatory condition associated to a long-term insulting infection and represents an underestimated CP key factor associated with an imbalance of pro-inflammatory and anti-inflammatory gene responses. The presence of a single nucleotide polymorphisms (SNPs) in the promoter region of interleukin 10 (IL-10) gene −1082, −819, and −592 was a possible determinant cause. This translational research aimed to provide outcomes on the role of IL-10 gene expression in bone loss diseases in patients affected by CP. Caucasian patients (n = 96) affected by CP were recruited from the Italian population. The subgingival samples were collected using the Bacterial Periodontal Assessment by Biomolecular Diagnostic® and the characterization of a set of 15 bacterial DNA responsible of periodontitis was performed by real-time multiplex PCR. In addition, two viruses, Epstein–Barr Virus (EBV) and Herpes Simplex Virus 1 (HSV-1), and a pathogenic fungi (Candida albicans) were included as a part of our panel. Our results confirmed an existing association between IL-10 gene polymorphisms and polymorphism of tumor necrosis factor alpha (TNFα), interleukin 1α-β-RN (IL-1α-β-RN), collagen type-l alpha (COLIA1), and vitamin D receptor (VDRs) genes in CP. Further studies are needed to improve diagnosis and endorse more effective therapeutic procedures for periodontal disease.

Highlights

  • Chronic periodontitis (CP) is a multi-factorial disorder that has showed to have a significant impact worldwide, according to recent outcomes places within the first six most prevalent chronic diseases worldwide, with more than 750 million people affected [1]

  • The interleukin 10 (IL-10) genotype frequencies of all investigated groups showed disequilibrium according to Hardy–Weinberg (p < 0.05)

  • The allele frequencies of the IL-10 gene polymorphisms were in accordance with Hardy–Weinberg equilibrium (p > 0.05)

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Summary

Introduction

Chronic periodontitis (CP) is a multi-factorial disorder that has showed to have a significant impact worldwide, according to recent outcomes places within the first six most prevalent chronic diseases worldwide, with more than 750 million people affected [1]. Different lines of evidence confirmed the primary role of MetS in increased periodontal inflammation due to the high presence of lipopolysaccharide (LPS) that immediately triggers an immune response. The experimental use of fat rats (a model of MetS) clearly confirmed the elusive high level of pro-inflammatory responses that evolved in individuals affected by both MetS and CP. The study clearly assessed the high presence of pro-inflammatory cytokines, such as the tumor necrosis factor-α (TNF-α), the granulocyte/macrophage colony-stimulating factor (GM-CSF) and the IL-6 released by the adipose tissue [2,3,4]

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